Kondo Effect on Mesoscopic Scale (Review)

Following the discovery of the Kondo effect the bulk transport and magnetic behavior of the dilute magnetic alloys have been successfully described. In the last fifteen years new directions have been developed as the study of the systems of reduced dimensions and the artificial atoms so called quantum dots. In this review the first subject is reviewed starting with the scanning tunneling microscope (STM) study of a single magnetic impurity. The next subject is the reduction of the amplitude of the Kondo effect in samples of reduced dimension which was explained by the surface magnetic anisotropy which blocks the motion of the integer spin nearby the surface. The electron dephasing and energy relaxation experiments are discussed with the possible explanation including the surface anisotropy, where the situation in cases of integer and half-integer spins is very different. Finally, the present situation of the theory of dynamical structural defects is briefly presented which may lead to two-channel Kondo behavior.Comment: 8 pages, submitted to the JPSJ Special Issue "Kondo effect -- 40 years after the Discovery

Size Dependence In The Disordered Kondo Problem

We study here the role randomly-placed non-magnetic scatterers play on the Kondo effect. We show that spin relaxation effects (with time $\tau_s^o$)in the vertex corrections to the Kondo self-energy lead to an exact cancellation of the singular temperature dependence arising from the diffusion poles. For a thin film of thickness $L$ and a mean-free path $\ell$, disorder provides a correction to the Kondo resistivity of the form $\tau_s^o/(k_FL\ell^2)\ln T$ that explains both the disorder and sample-size depression of the Kondo effect observed by Blachly and Giordano (PRB {\bf 51}, 12537 (1995)).Comment: 11 pages, LaTeX, 2 Postscript figure

Electron dephasing near zero temperature: an experimental review

The behavior of the electron dephasing time near zero temperature, $\tau_\phi^0$, has recently attracted vigorous attention. This renewed interest is primarily concerned with whether $\tau_\phi^0$ should reach a finite or an infinite value as $T \to$ 0. While it is accepted that $\tau_\phi^0$ should diverge if there exists only electron-electron (electron-phonon) scattering, several recent measurements have found that $\tau_\phi^0$ depends only very weakly on temperature, if at all, when $T$ is sufficiently low. This article discusses the current experimental status of "the saturation problem", and concludes that the origin(s) for this widely observed saturation are still unresolved

Spin-Orbit-Induced Magnetic Anisotropy for Impurities in Metallic Samples I. Surface Anisotropy

Motivated by the recent measurements of Kondo resistivity in thin films and wires, where the Kondo amplitude is suppressed for thinner samples, the surface anisotropy for magnetic impurities is studied. That anisotropy is developed in those cases where in addition to the exchange interaction with the impurity there is strong spin-orbit interaction for conduction electrons around the impurity in the ballistic region. The asymmetry in the neighborhood of the magnetic impurity exhibits the anisotropy axis $n$ which, in the case of a plane surface, is perpendicular to the surface. The anisotropy energy is $\Delta E=K_d (nS)^2$ for spin $S$, and the anisotropy constant $K_d$ is inversionally proportional to distance $d$ measured from the surface and $K_d>0$. Thus at low temperature the spin is frozen in a singlet or doublet of lowest energy. The influence of that anisotropy on the electrical resistivity is the subject of the following paper (part II).Comment: 28 pages, RevTeX (using epsfig), 8 eps figures included, submitted to PR

Hexokinase II Detachment from Mitochondria Triggers Apoptosis through the Permeability Transition Pore Independent of Voltage-Dependent Anion Channels

Type II hexokinase is overexpressed in most neoplastic cells, and it mainly localizes on the outer mitochondrial membrane. Hexokinase II dissociation from mitochondria triggers apoptosis. The prevailing model postulates that hexokinase II release from its mitochondrial interactor, the voltage-dependent anion channel, prompts outer mitochondrial membrane permeabilization and the ensuing release of apoptogenic proteins, and that these events are inhibited by growth factor signalling. Here we show that a hexokinase II N-terminal peptide selectively detaches hexokinase II from mitochondria and activates apoptosis. These events are abrogated by inhibiting two established permeability transition pore modulators, the adenine nucleotide translocator or cyclophilin D, or in cyclophilin D knock-out cells. Conversely, insulin stimulation or genetic ablation of the voltage-dependent anion channel do not affect cell death induction by the hexokinase II peptide. Therefore, hexokinase II detachment from mitochondria transduces a permeability transition pore opening signal that results in cell death and does not require the voltage-dependent anion channel. These findings have profound implications for our understanding of the pathways of outer mitochondrial membrane permeabilization and their inactivation in tumors

Concentration Dependent Ion Selectivity in VDAC: A Molecular Dynamics Simulation Study

The voltage-dependent anion channel (VDAC) forms the major pore in the outer mitochondrial membrane. Its high conducting open state features a moderate anion selectivity. There is some evidence indicating that the electrophysiological properties of VDAC vary with the salt concentration. Using a theoretical approach the molecular basis for this concentration dependence was investigated. Molecular dynamics simulations and continuum electrostatic calculations performed on the mouse VDAC1 isoform clearly demonstrate that the distribution of fixed charges in the channel creates an electric field, which determines the anion preference of VDAC at low salt concentration. Increasing the salt concentration in the bulk results in a higher concentration of ions in the VDAC wide pore. This event induces a large electrostatic screening of the charged residues promoting a less anion selective channel. Residues that are responsible for the electrostatic pattern of the channel were identified using the molecular dynamics trajectories. Some of these residues are found to be conserved suggesting that ion permeation between different VDAC species occurs through a common mechanism. This inference is buttressed by electrophysiological experiments performed on bean VDAC32 protein akin to mouse VDAC

Differential Cerebral Cortex Transcriptomes of Baboon Neonates Consuming Moderate and High Docosahexaenoic Acid Formulas

BACKGROUND: Docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (ARA, 20:4n-6) are the major long chain polyunsaturated fatty acids (LCPUFA) of the central nervous system (CNS). These nutrients are present in most infant formulas at modest levels, intended to support visual and neural development. There are no investigations in primates of the biological consequences of dietary DHA at levels above those present in formulas but within normal breastmilk levels. METHODS AND FINDINGS: Twelve baboons were divided into three formula groups: Control, with no DHA-ARA; “L”, LCPUFA, with 0.33%DHA-0.67%ARA; “L3”, LCPUFA, with 1.00%DHA-0.67%ARA. All the samples are from the precentral gyrus of cerebral cortex brain regions. At 12 weeks of age, changes in gene expression were detected in 1,108 of 54,000 probe sets (2.05%), with most showing <2-fold change. Gene ontology analysis assigns them to diverse biological functions, notably lipid metabolism and transport, G-protein and signal transduction, development, visual perception, cytoskeleton, peptidases, stress response, transcription regulation, and 400 transcripts having no defined function. PLA2G6, a phospholipase recently associated with infantile neuroaxonal dystrophy, was downregulated in both LCPUFA groups. ELOVL5, a PUFA elongase, was the only LCPUFA biosynthetic enzyme that was differentially expressed. Mitochondrial fatty acid carrier, CPT2, was among several genes associated with mitochondrial fatty acid oxidation to be downregulated by high DHA, while the mitochondrial proton carrier, UCP2, was upregulated. TIMM8A, also known as deafness/dystonia peptide 1, was among several differentially expressed neural development genes. LUM and TIMP3, associated with corneal structure and age-related macular degeneration, respectively, were among visual perception genes influenced by LCPUFA. TIA1, a silencer of COX2 gene translation, is upregulated by high DHA. Ingenuity pathway analysis identified a highly significant nervous system network, with epidermal growth factor receptor (EGFR) as the outstanding interaction partner. CONCLUSIONS: These data indicate that LCPUFA concentrations within the normal range of human breastmilk induce global changes in gene expression across a wide array of processes, in addition to changes in visual and neural function normally associated with formula LCPUFA